Metabolic syndrome is a pathologic condition in which a visceral fat accumulation amount increases by lifestyle habits and hereditary predisposition, with the result that insulin resistance is induced and symptoms such as lipidosis, hypertension and impaired glucose tolerance emerge and a vascular lesion is likely to occur. Such pathologic condition leads to arteriosclerosis such as cardial infarction and cerebral infarction and at worst may result in death.
When insulin resistance emerges due to metabolic syndrome, the function of the vascular endothelial cells is damaged. As a cause thereof, abnormality of the nitrogen monoxide (hereinafter, simply referred to as NO) production system in the vascular endothelial cells is suggested (Non Patent Literature 1).
NO is produced by L-arginine and an oxygen molecule by endothelial NO synthetase (hereinafter, simply referred to as eNOS) in the vascular endothelial cells. The role of NO, which is a vascular relaxation factor derived from the vascular endothelium, is primarily a suppressive action on proliferative change, inflammatory change, platelet aggregation and oxidation stress. A reduction of NO production and insufficient action thereof were observed in the presence of various risk factors such as arteriosclerosis and hyperlipemia (Non Patent Literature 2). Particularly, in the state of insulin resistance associated with metabolic syndrome, it is known that the activity of GTP cyclohydrase I (hereinafter, simply referred to as GTP-CH1), which is a coenzyme of eNOS, i.e., a tetrahydrobiopterin (hereinafter, simply referred to as BH4) producing enzyme, reduces (Non Patent Literature 1). Mechanism of reduction of NO production and insufficient production thereof is complicated; however, it is known that eNOS activity is inhibited by a metabolite of L-arginine, asymmetric dimethyl arginine (hereinafter, simply referred to as ADMA). Furthermore, in the state where eNOS activity reduces, oxygen molecules are preferentially metabolized by NADPH oxidase to generate active oxygen, which further induces hypoactivity of vascular endothelium (Non Patent Literature 3). On the other hand, when vascular endothelial cells produce ADMA degrading enzyme, i.e., dimethylarginine dimethylaminohydrolase 2 (hereinafter, simply referred to as DDAH 2), the vascular endothelial function can be satisfactorily maintained. Furthermore, the vascular endothelial function can be satisfactorily maintained also by reducing NADPH oxidase activity present in the vascular endothelial cells.
A food material having a vascular endothelial function improving effect, (−)-epigallocatechin-3-O-gallate (hereinafter, also referred to as “EGCG”) contained in green tea is known (Non Patent Literature 4). Furthermore, it is reported that when black tea is taken, the vasodilation depending upon blood flow of the human upper arm is improved (Non Patent Literature 5), that eNOS activation is facilitated in the in-vitro study using a black tea extract (Non Patent Literature 6); however, active ingredients thereof did not elucidated. Furthermore, no study has been made on oolong tea and its components.
Examples of the EGCG polymer produced by an oolong tea intrinsic fermentation process include a dimer (oolong homobisflavan A and oolong homobisflavan B)(Non Patent Literature 7) and a trimer (Patent Literature 1) have been isolated and identified. It has been reported that these compounds have strong pancreatic lipase inhibitory activity (Non Patent Literature 8 and Patent Literature 1).